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. 2016 Feb 27;23:30. doi: 10.1186/s12929-016-0229-4

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© Chen et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 9 — The immunofluorescence localization of TβR-II-HA and caveolin-1 in Mv1Lu cells treated with and without BetA. The Mv1Lu cells transiently expressing TβR-II-HA were treated with or without 5 μg/mL of BetA at 37 °C for 1 h. The cells were then fixed with cold methanol and incubated with a mouse antibody against HA (panels a and b) and a rabbit antibody against caveolin-1 (panels b and e), followed by incubation with Rhodamine-conjugated donkey anti-mouse antibody or FITC-conjugated goat anti-rabbit antibody. Fluorescence in cells was examined using a confocal microscope: Bar, 20 μm. The white arrows indicate the colocalization of TβR-II-HA and caveolin-1 at the cell surface and endocytic vesicle (panel c, enlarged picture in lower right corner.) before BetA treatment. (panel f, enlarged picture in upper right corner.) BetA treatment reduces the colocalization of TβR-II-HA and caveolin-1